The phenomenon which manifests as growth arrest after a period of apparently normal cell proliferation is known as Replicative Senescence (RS). Replicative Senescence is seen in a) cells from adults of all ages b) embryonic tissues, and c) animals.
Aging is associated with alterations of the immune system including impairments in innate immunity, T-lymphopoiesis and B-lymphopoiesis and these impairments contribute to immunosenescence and immune dysfunction in affected individuals. Multipotent hematopoietic stem cells (HSCs) aging contributes to impairments in early lymphoid lineage differentiation. Immunosenescence with immune dysfunction and increased inflammation is a primary cause of aging and diseases such as anemia, chronic diseases, autoimmune disorders, cancer, cardiovascular diseases, infection, metabolic diseases, neurodegenerative diseases, protein energy malnutrition and frailty.
Oscillating magnetic fields have been used for years in the course of administering physical therapy to clinic patients suffering from bone fractures. These devices are typically called bone growth stimulators. Bone growth occurs as a result of stem cell stimulation, activation and differentiation. These device signals, however, are a series of pulses or oscillating waves, which have symmetry typical of electronic-generated signals (see FIG. 1 “Common electronic-generated signals”). More recently, researchers have discovered that the body emits its own complex electromagnetic field pattern. Unique patterns are associated with immunosenescence and immune dysfunction, stress, or disease. By capturing these abnormal patterns, re-storing and re-admitting these patterns to the target patient, researchers theorize that the normal “healing process” may be restored more effectively, as the patterns would be natural biologic patterns.
What is unique about the instantly disclosed method described is the confluence of these unique processes to promulgate a therapeutic modality.
The number of Cumulative population doublings (CPDs) cells undergo in culture varies considerably between cell types and species. Early results suggested a relation between CPDs cells could endure and the longevity of the species from which the cells were derived, e.g. cells from the Galapagos tortoise, which can live over a century, divide about 110 times while mouse cells divide roughly 15 times. Cells taken from patients with progeroid syndromes such as Werner syndrome (WS)—exhibit far fewer CPDs than normal humans. Certain “immortal” cell lines can divide indefinitely without reaching RS, e.g. embryonic germ cells and most cell lines derived from tumors, such as HeLa cells.
Biomarkers of cell senescence include:                1) Growth arrest—Senescent cells are growth arrested in the transition from phase G1 to phase S of the cell cycle. The growth arrest in RS is irreversible in the sense that growth factors cannot stimulate the cells to divide even though senescent cells can remain metabolically active for long periods of time;        2) Cellular morphology—Senescent cells are bigger and a senescent population has more diverse morphotypes than cells at earlier CPDs (Note FIG. 12 which shows Normal human fibroblasts (left) and fibroblasts showing a senescent morphology (three cells on the right). Notice the common elongated morphology of senescent cells.        3) Senescence-associated β-galactosidase (SA β-gal) activity—In vitro and in vivo, the percentage of cells positive for SA β-gal increases with, respectively, CPDs and age. In immortal cell lines, such as HeLa tumor cells, the percentage of cells positive for SA β-gal does not correlate with CPDs. The increase in SA β-gal also correlates with the appearance of the senescent morphotypes;        4) Polyploid Increase—the percentage of polyploid cells—i.e., cells with three or more copies of chromosomes—has been shown to increase. Deletions in the mitochondrial DNA (mtDNA) have also been observed both during RS and during aging in vivo, at least in some cells;        5) Change in Gene Expression Levels—The expression levels of several genes change during in vitro cellular aging One important type of gene overexpressed in senescent cells are inflammatory regulators like interleukin 6 (IL6); proinflammatory proteins secreted by senescent cells in driving senescence, which may lead to positive feedback loops and to senescence induction in normal cells near senescent cells;        6) Metalloproteinase and Heat Shock Protein Production—Senescent cells also display an increased activity of metalloproteinases which degrade the extracellular matrix and a decreased ability to express heat shock proteins;        7) Telomere shortening—the primary cause of RS in human fibroblasts which have a major role in aging.        